| 要旨： |
Lymphocyte activation leads to rapid proliferation and differentiation and we have shown that CD4 T cell subsets are metabolically distinct. These metabolic distinctions may allow new understanding and approaches to manipulate immunity. We show that T cells in Renal Cell Carcinoma are metabolically suppressed and that improving metabolism can improve T cell function. Glut1 is a member of the glucose transporter family, of which T cells express several members. We have shown that while effector T cells require Glut1 and aerobic glycolysis to promote immunity, Treg can function independent of Glut1 to suppress Inflammatory Bowel Disease (IBD). In addition, T cells consume glutamine through Glutaminase and we show that this metabolic pathway is differentially utilized by effector T cell subsets. Understanding mechanisms that regulate T cell metabolism may provide new tools to modulate immunity the balance of T cell effector and regulatory populations. |
